pH gradient and distribution of streptococci, lactobacilli, prevotellae, and fusobacteria in carious dentine
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Caries process comprises acidogenic and aciduric bacteria that are responsible for lowering the pH and subsequent destruction of hydroxyapatite matrix in enamel and dentine. The aim of this study was to identify the correlation between the pH gradient of a carious lesion and proportion and distribution of four bacterial genera; lactobacilli, streptococci, prevotellae, and fusobacteria with regard to total load of bacteria.
Materials and methods
A total of 25 teeth with extensive dentinal caries were sampled in sequential layers. Using quantitative real-time PCR of 16S rRNA gene, we quantified the total load of bacteria as well as the proportion of the above-mentioned genera following pH measurement of each sample with a fine microelectrode.
We demonstrated the presence of a pH gradient across the lesion with a strong association between the quantity of lactobacilli and the lowest pH range (pH 4.5–5.0; p = 0.003). Streptococci had a tendency to occupy the most superficial aspect of the carious lesion but showed no correlation to any pH value. Prevotellae showed clear preference for the pH range 5.5–6.0 (p = 0.042). The total representation of these four genera did not reach more than one quarter of the total bacterial load in most carious samples.
We revealed differential colonization behavior of bacteria with respect to pH gradient and a lower than expected abundance of lactobacilli and streptococci in established carious lesions. The data indicate the numerical importance of relatively unexplored taxa within the lesion of dentinal caries.
The gradient nature of pH in the lesion as well as colonization difference of examined bacterial taxa with reference to pH provides a new insight in regard to conservative caries management.
KeywordsCaries Real-time PCR Gram-positive bacteria Gram-negative bacteria pH gradient 16S rRNA
The authors acknowledge funding from NIH/NIDCR (grant no. R01 DEO15272-07), Australian National Health and Medical Research Council (NHMRC grant no. 512524.3), Australian Dental Research Foundation (grant no. 91–2011]), and New South Wales Dental Board (grant no. 2011). We thank Dr Derek Harty and Dr Mangala Nadkarni (Institute of Dental Research, Westmead, NSW, Australia) for provision of some DNA materials. We also thank Mr. Mitchell Brown and Mr. Terry Flood (Center for Infectious Disease and Microbiology, Institute for Clinical Pathology and Medical Research, Westmead, Australia) who provided us with valuable assistance with culture and magnetic DNA extraction of some bacteria.
Conflict of interest
The authors declare no potential conflicts of interest in regard to authorship and/or publication of this article.
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